2. Cellular Injury and Adaption Flashcards

1
Q

What is the most common cause of injury at the cellular level?

A

Hypoxia.

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2
Q

What is hypoxia?

A

It is the lack of oxygen that leads to the inability of the cell to synthesize suficient ATP by aerobic oxidation.

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3
Q

What is the most common cause of hypoxia?

A

Ischemia.

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4
Q

What is isquemia?

A

It is the loss of blood supply due to decreased arterial flow or decrease venous outflow.

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5
Q

What is the most common mode of inheritance reguarding genetic defects involving enzymes ?

A

Recessive manner.

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6
Q

What is the most common mode of inheritance reguarding genetic defects involving structural proteins?

A

Dominant manner.

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7
Q

What does Vitamin A deficiency lead to?

A

Night blindness, squamous metaplasia, immune deficiency.

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8
Q

What does Vitamin C deficiency lead to?

A

Scurvy.

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9
Q

What does Vitamin D deficiency lead to?

A

Rickets and osteomalacia.

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10
Q

What does Vitamin K deficiency lead to?

A

Bleeding Diathesis.

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11
Q

What does Vitamin B12 deficiency lead to?

A

Megaloblastic anemia, neuropathy, and spinal cord degeneration.

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12
Q

What does Folate deficiency lead to?

A

Megaloblastic anemia and neural tube defect.

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13
Q

What does Niacin deficiency lead to?

A

Pellagra (diarrhea, dermatitis, and dementia). [N-word:3D’s]

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14
Q

What are the four protective factors against free radicals?

A

Antioxidants, Superoxide dismutase, glutathione peroxidase, catalase.

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15
Q

What does release of cytochrome C inside the mitochondria do?

A

Trigger fo apoptosis.

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16
Q

What is pyknosis?

A

Degeneration and condensation of nuclear chromatin

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17
Q

What is karyorrhexis?

A

Nuclear fragmentation.

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18
Q

What is Karyolysis?

A

Dissolution of the nucleus.

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19
Q

What clinical marker is released during biliary tract obstruction?

A

Alkaline phosphatase.

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20
Q

What clinical marker is released during hepatitis?

A

Transaminases.

21
Q

What clinical marker is released during pancreatitis?

A

Amylase and lipase.

22
Q

What clinical marker is released during myocardial injury?

A

Creatine phosphokinase-MB isozyme (CPKMB, lactate dehydrogensase [LDH], Troponin).

23
Q

In what type of cellular injury do we observe massive influx of calcium?

A

Irrevesible cell injury.

24
Q

What is the most common form of necrosis?

A

Coagulative necrosis.

25
Q

What is coagulative necrosis?

A

Denaturing and coagulation of proteins within the cytoplasm, micro: loss of nucleus but preservation of cellular shape. Common in most organs including the heart, liver, and kidney.

26
Q

What is liquefactive necrosis?

A

Cellular destruction by hydrolytic enzymes, due to autolysis and heterolysis. Occurs in absecesses, brain infarcts and pancreatic necrosis.

27
Q

What is caseous necrosis?

A

Combination of coagulatoin and liquefaction necrosis, gross: soft, friable, and cottage-cheese like. Characteristic of tuberculosis.

28
Q

What is fat necrosis?

A

Caused by the action of lipase on fatty tissue. It has a chalky white apperance.

29
Q

What is fibrinoid necrosis?

A

Necrotic tissue that histologically resembles fibrin. Micro: has an eosinophilic (pink) homogenous apperance.

30
Q

What is gangrenous necrosis?

A

It is a gross term used to describe dead tissue. Common sites are lower limbs, gallbladder, GI tract, and testes.

31
Q

What is Dry gangrene?

A

Microscopic pattern is coagulative necrosis.

32
Q

What is Wet gangrene?

A

Microscopic pattern is liquefactive necrosis.

33
Q

What is apoptosis and what is special about it?

A

It is programmed cell death; there is a lack of an inflammatory response.

34
Q

What gene inhibits apoptosis?

A

It is the bcl-2; it prevents release of cytochrome c from mitochondria and binds pro-apoptotic protease activating factor (Apaf-1).

35
Q

What gene stimulates apoptosis?

A

It is p-53; it is elevated by DNA injury and arrests the cell cycle. If DnA repair is impossible, p53 stimulate apoptosis.

36
Q

How is apoptosis executed?

A

Mediated by a cascade of caspases; they digest nuclear and cytoskeletal proteins and activate endonucleases.

37
Q

What are Councilman bodies?

A

It is an eosinophilic globule often surrounded by normal parenchyma found in the liver of individuals suffering from viral hepatitis, yellow fever, or other viral syndrome. It represents a hepatocyte that is undergoing apoptosis.

38
Q

What is atrophy?

A

It is the decrease in cell size and funtional ability. Micro: small shrunken cells with lipofuscin granules. EM: decreased intracellular components, and autophagosomes.

39
Q

What is hypertrophy?

A

An increase in cell size and functional ability due to increased synthesis of intracellular components.

40
Q

What is hyperplasia?

A

An increase in the number cells in a tissue or organ.

41
Q

What is metaplasia?

A

A reversible change of one cell type to another, usually in response to irritation.

42
Q

What is dysplasia?

A

An abnormal proliferation of cells that is characterized by changes in cell size, shape, and loss of cellular organization; it is not cancer but may progress to cancer (preneoplastic lesion) like cervial dysplasia.

43
Q

What is a Russell body?

A

It is a intracytoplasmic accumulation of immunoglobulins in plasma cells.

44
Q

What is Lipofuscin?

A

It is an endogenous pigment of wear and tear pigment that is perinuclear yellow-brown pigement. It is an indigestible material within lysosomes, common in the liver and heart.

45
Q

What is hyaline change?

A

A nonspecific term used to describe any intracellular or extracellular alteration that has a pink homogenous appearance on H and E stains.

46
Q

What is dystrophic calcification?

A

Precipitation of calcium phosphate in dying or necrotic tissues.

47
Q

What is a Psammoma body?

A

There are laminated calcifications that occur in meningiomas and papillary carcinomas of the thyroid and ovary.

48
Q

What is metastatic calcification?

A

Precipitation of calcium phosphate in normal tissue due to hypercalcemia (supersaturated solution).